Megaloblastic anaemias (MA) are frequently associated with
haemolysis. The pathogenesis of these finding is not clear, but it is thought to depend on the greater destruction of abnormal and fragile megaloblastic erythrocytes.
Vitamin B(12) and
folate deficiencies are the commonest cause of MA; these deficiencies may simultaneously induce a significant alteration in
homocysteine metabolism leading to
hyperhomocysteinemia. Blood cells have
enzymes involved in
homocysteine metabolism. Considering the possible effects of
hyperhomocysteinemia in erythrocyte toxicity (due to oxidative damage and/or to interaction with sulfhydryl residues of structural and enzymatic
proteins), the aim of our study was to evaluate (1) the
homocysteine blood cells production in patients with MA due to
vitamin B(12) and
folate deficiency and (2) the possible role and mechanism of
hyperhomocysteinemia in MA
haemolysis. After incubation at 37 degrees C, blood samples from MA patients showed higher and significant levels of Hcy, LDH, lipid peroxidation parameters (MDA), and ghost
protein-bound Hcy than controls.
Haemolysis (%) was higher in MA patients than controls and was significantly correlated with Hcy accumulation in the medium, lipid peroxidation indices and ghost
protein-bound Hcy. No significant (or significantly lower) alterations through time in considered parameters were observed in the corresponding samples incubated at 4 degrees C or in samples incubated with
methionine-free medium (lower Hcy production). Our data, deriving from an in vitro experience, suggest a possible role of Hcy accumulation due to
vitamin B(12) and
folate deficiencies in
haemolysis associated to MA due to
vitamin deficiency.